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89 Cards in this Set

  • Front
  • Back
Viral Structure:
-may be absent
-from the host cell
Envelope
Viral Structure:
-between envelope and capside
Matrix Protein
Viral Structure:
-surrounds nucleic acid
-RNA or DNA (not both)
-single or double stranded
Capsid
4 Modes of Virus Infection
1. get it, get over it, immune
2. get it, get over it, get it again
3. get it, latent
4. get it, chronic
Interferon:
-induce synthesis of DAI
-double stranded RNA- activated inhibitor of translation = RNA dependent protein kinase
-DAI binds to double stranded RNA and is activated
-inactivates a gene required for protein synthesis
-prevents synthesis of new virus by inhibiting ALL protein synthesis in the infected host cell
Interferon alpha and beta
Interferon:
-directly inhibits viral replication
-binds to specific cell receptors
-STAT signaling -> synthesis of antiviral proteins
-inhibits viral polymerase activity
-stimulates MHC I activity, activates NK cells
Interferon gamma
Cells:
-cytotoxic to virus infected cells
-controls primary infection, before primary T cells
-stimulated by IL 12
NK cells
-initiated by classical or alternative
-damage viral envelope
-block viral receptor
-direct virolysis
-opsonization of coated virus or of infected cells leading to phagocytosis
-lysis of infected cells
Complement
Virus:
-retrovirus
-outer evelope of lipid bilayer from the cell in which it develops, with embedded viral proteins
-matrix protection between envelope and core
-RNA surrounded by a protein capsid
HIV
molecule on HIV surface that binds to CD$ molecules on cell surfaces
gp120
fusigenic domain molecule on HIV
gp41
antibody development for HIV is not available, why?
access for gp41 is covered with gp120
__________ of HIV viral RNA into DNA occurs in cell's cytoplasm
reverse transcription
Modes of HIV leaving the cell
1. budding
2. synctial formation (cell-to-cell)
HIV evasion strategies:
1. antigenic variation
2. hide in CNS or FDC, not exposed to antibody
3. decrease MHC I class I expression in infected cells
Virus:
-hepadnaviruses
-double stranded DNA viruses with envelope proteins
-outer envelope of surface
-inner core with protein coat
-viral DNA
-DNA polymerase
Hepatitis B
Virus Antigens:
-for Hep B, one of the first things detected in bloodstream
-as soon as one week after infection
Hep. B DNA and Hep. B DNA polymerase
Virus Antigens:
-for Hep B
-not detectable in laboratory assays
Hep. B core proteins (HBcAg)
Virus Antigens
-for Hep B
-6-25 weeks to appear
-appears only after viral replication
-if present for more than 6 months, chronic infection
Hep. B surface proteins (HBsAg)
Virus Antigens:
-for Hep B
-detectable when virus actively producing
Hep. B envelope proteins (HBeAg)
Antibodies:
-Hep B
-first detectable, about 8 weeks
-indicates infection rather than vaccination
Anti-Hep B core (HBcAb)
Antibodies:
-Hep B
-normally appears after antigen no longer detectable
Anti-Hep B envelope (HBeAb)
Antibodies:
-Hep B
-marker of immunity
-you are cured
Anti-Hep B surface (HBsAb)
Hepatitis B patient with:
-HBsAg and HBeAg
-No HBsAb and HBeAb
Chronic Carrier
Virus:
-has Hep B surface antigens and needs Hep B
Hepatitis D
Virus:
-flaviridae
-hepacivirus (ssRNA)
Hepatitis C
Definition:
-refers to genetic heterogeneity among different HCV isolates within a population
-vary by 31-35% of nucleotides over the entire length of the genome
HCV Genotype
Definition:
-refers to genetic heterogeneity of the HCV isolates within on individual
-vary by 1-9% of nucleotides
HCV Quasispecies
HCV testing:
-similar to Western Blot
-look for antibody to a battery of recombinant antigens on a plastic strip
Recombinant Immunoblast Assay (RIBA)
Virus:
-flavivirus; close relative to Hep C
-not causes hepatitis always
Hepatitis G
Virus:
-picornavirus
-acute disease and asymptomatic infection
-no chronic infection
Hepatitis A
Virus:
-possible caliciviridae
-ssRNA
-found in swine worldwide
Hepatitis E
Hepatitis E genotypes, found in humans
Types 1 and 2
Hepatitis E genotypes, found in humans and swine
Types 3 and 4
Hepatitis E genotypes, found in avian
Type 5
Hepatitis viruses with vaccines
Hepatitis A and B (technically D)
Hepatitis viruses transmitted in the blood
Hepatitis B, C, and D
Hepatitis viruses transmitted in the feces
Hepatitis A and E
Virus:
-orthomyxoviridae
-types A (human and other animals)
-types B (human)
Influenza
Influenza protein:
-glycoprotein mediates receptor binding (initial step in infection)
Hemagglutinin
Influenza protein:
-protein facilitates mobility of virions
Neuraminidase
Influenza antibody to _____ is neutralizing antibody
(prevents infection)
Hemagglutinin
Influenza antibody to _____ is infection permissive but disease suppressive
(partial suppression of viral load)
(lower amounts of virus)
Neuraminidase
-point mutations in influenza result in variation in protein composition
-changes in antigenic structure
-loss of prior antibody match
Antigenic Drift
-recombination of different strain genomes of influenza
-new types of Hemagglutinin or Neuraminidase in a virus with a human transmissivity
-infected by two different viruses
Antigenic Shift
-Mediates virus transmissibility of the hemaglutinin membrane glycoprotein binding to _____ on cell surfaces
-changes in binding specificity may be required for effective cross species transfer
Sialic Acids
-Avian strains of influenza bind preferentially to _____
-common only in alveoli in humans
alpha 2,3
-Human strains of influenza bind preferentially to _____
-common in nose and throat in humans
alpha 2,6
-Swine strains of influenza bind preferentially to _____
alpha 2,6 and 2,3
Viruses:
-ds DNA viruses
-replicate and assemble in the nucleus
-glycoprotein envelope
-complex viruses: ~35 virion proteins
-variations with animal species
-modulate host immune response through latent infections and secrete "versions" of cellular cytokine receptors
Herpes Viruses
Viruses:
-HSV1, HSV2 herpes (cold sores, gential ulcers)
-Varicellovirus (VZV) (chicken pox, shingles
Alpha Herpes Viruses
-secreted by alphaviruses
-degradation of host mRNA and shutoff of host protein synthesis in non-neuronal cells
-promotes efficient virus replication
-neurons are resistant, leads to latent infection
Virion Host Shut Off protein (VHS)
-alpha herpes viruses
-promote neuronal survival by inhibitory apoptosis
Latency Associated Transfer protein (LAT)
Viruses:
-Cytomegalovirus (CMV)
-Roseolovirus (HHV-6, HHV-7)
-nearly universal infection, generally asymptomatic
-produces protein that binds MHC I preventing it from being expressed on the infected cell surface
Beta Herpes Viruses
Virus:
-infection leads to polyclonal B cell activation and proliferation
-once infected, lifelong carrier state develops
-low grade virus replication and shedding in the epithelial cells of the pharynx of all seropositive individuals
-able to immortablize B lymphocytes in vitro and in vivo
Epstein Barr Virus (EBV)
EBV disease:
-primary infection, usually subclinical in childhood
-self limited
-complications are rare
-chronic IM may occur, death due to lymphoma
-(spread by kissing)
Mononucleosis
EBV disease:
-endemic in parts of Africa and Papa New Guinea
-restricted to areas endemic with malaria, a cofactor
-degranulation of the c-myc gene
Burkitt's Lymphoma
EBV disease:
-malignant tumor of the squamous epithelium of the nasopharynx
-prevalent in South China
-patients have high titers of antibodies against various EBV antigens
Nasophayngeal Carcinoma
EBV disease:
-immunocompromised patients
Lymphoma
Virus:
-gamma herpes virus
-associated with Kaposi's Sarcoma (AIDS) and B Cell lymphomas
-KS with antibodies
-viral oncogenes present but are kept under immunological control; problem during immunosuppression
HHV-8
Viruses:
-arthropod borne viruses
Arboviruses
Viruses:
-ssRNA
-3 structural proteins in viral capsid with host derived lipid bilayer: capsid, membrane, envelope
-acidic endosome leads to trimerization of E proteins which leads to viral and cellular membranes
-JE, SLE, WN
Flaviviridae
Virus:
-transmitted by Aedes aegypti
Dengue
-for Dengue, infection in an individual who has pre-existing antibody to a closely related agent elicits both hemotype (to the current infecting strain) and heterotype (first infected strain) antibody development
-cross reacting antigens react with and stimulate clones with high avidity for the original antigen
Original Antigenic Sin
Dengue Disease:
-primary infection with one strain results in antibody development to that strain
-this antibody is neutralizing for the primary infection but not the other three
-antibody binds to virus from a second infecting strain and enhances binding to the Fc receptors on the cell surface
-enhances virus uptake by macrophages, infected
-hyperactivates the complement system, histamine, TNF, thromboplastin
-leads to cell lysis, vascular permeability
Dengue Hemorrhagic Fever
Interpretation of clinical Specimens Serology for SLE, DEN, and WN:
low+ IgM
- IgG
very acute infection or false +
Interpretation of clinical Specimens Serology for SLE, DEN, and WN:
++ IgM
+- IgG
recent infection
Interpretation of clinical Specimens Serology for SLE, DEN, and WN:
low+ IgM
++ IgG
secondary infection with a related virus or early convalescent serum
Interpretation of clinical Specimens Serology for SLE, DEN, and WN:
- IgM
+ IgG
infection in the past with a related virus
4 Benefits of Vaccines
1. disease prevention
2. reduction of disease severity
3. outbreaks prevention for contagious disease
4. herd immunity
Definition:
-protected from disease if exposed
Immune
Definition:
-protection generated by person's own immune system; results from infectious or vaccination, may include cell mediated immune response
Active Immunity
Definition:
-protective factors (pre-formed) antibodies from one animal are transferred to another
Passive Immunity
3 Problems with Passive Immunity:
1. does not active immune response, no cellular component
2. does not generate memory response
3. serum sickness
Type of Vaccine:
-antigen must be large enough and with correct shape to elicit antibody response
-bacterial polysaccharide
-activate B cells, leads to IgM (no affinity maturation, no class switiching)
-require conjugation to carrier to work well
-polysaccharide-protein conjugate is more immunogenic
-activates TH cells
-enables class switching (IgM to IgG)
-may activate some memory cells
Surface Antigens Subcellular
Type of Vaccine:
-very effective but boosters required to maintain immunity
-tetanus and diphtheria combined
-filtrate of bacterial cell culture is treated with formaldehyde, adsorbed onto aluminum salt and thimerosol added as a preservative
Toxin/Toxoid Vaccines
Type of Vaccine:
-clone gene for antigen, insert into cell to produce large amounts of antigen which is used as vaccine
-insert gene for antigen into a non-virulent virus or bacterium which acts as a vector to infect host and produce antigen in situ
-direct inoculation of agent DNA
Recombinant DNA/RNA
Type of Vaccine:
-cannot initiate an infection, does not replicate
-usually needs multiple doses
-antibody titer drops over time
-polyantigenic
-adverse effects mostly local inflammatory
Killed/Inactivated Vaccines
Type of Vaccine:
-goal of attenuation: diminish virulence while retaining antigenicity
-many sequential passages in host system with selection for decreased virulence
-causes infection similar to natural infection, but not disease
-maybe neutralized by antibody already present in recipient
-danger to immunocompromised recipient
-adverse effect similar to mild natural illness
-can transfer agent to others, resulting in spend of vaccine agent
-potential for reversion to the wild type through mutation or reassortment of genes
Live/Attenuated Vaccines
Definitions:
-added vaccines to increase immune response, stimulate inflammatory response
-activate DCs through Toll-like receptors
-immune stimulating complexes (ISCOMS)
-concentrate antigen at a site where are exposed to it and induce cytokine production
-aluminum salts, Freund's complete, Bordetella perussis
Adjuvants
Definition:
-some vaccines require multiple doses over time to achieve adequate levels of immunity
-secondary antibody response has shorter lag phase and extended plateau and decline
-secondary antibody response plateau is higher than primary response plateau
-secondary antibody response primarily IgG
-secondary antibody response has higher affinity
-the role of memory cells to immunity is related to incubation period of the pathogen
-if very short, disease symptoms are present by the time memory cells activated (must maintain high levels of neutralizing antibody by repeat immunization)
Boosters
when multiple doses are required, increase the time interval _____ vaccine effectiveness
does not reduce
when multiple doses are required, decrease the time interval _____ vaccine effectiveness
reduce
6 Strategies Organisms Use to Evade Immunity Response
1. antibody is made to epitopes, but not to genetic material of the organism
2. limited viremia on bacteremia
3. cell mediated response required for protection
4. hides in an inactive state inside cells
5. integration with host cell genome (retroviruses)
6. bacteria: surface antigen covered by capsule which is not immunogenic
If mother is HBsAg +: administer _____
Hep B vaccine and HBIG (immune globulin) within 12 hours of birth at separate sites
If mother is HB unknown: administer _____
Hep B vaccine within 12 hours of birth and test mother; if + give HBIG (immune globulin)
If mother is HBsAg -: administer _____
vaccine within 2 months
Why do we still have disease for which vaccine exist?
-cost, delivery system, political/religious issues
-vaccine side effects
-suboptimal vaccine effectiveness
Why do we still have diseases with no available vaccines
-many life stages and antigenic variation
-parasite cell components are like "self", auto-immune response
-cause immunosuppression or multiply in immune system cells
-ignorance of effective immunity
-multiple serotypes
-risk of reversion and reactivation of agent
-variation in antigen over time